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White lesions (2)

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  • 1. GOOD AFTERNOON Dr.Rajesh
  • 2. LESIONS
  • 3. Macules •Well-circumscribed, flat lesions that are noticeable because of their change from normal skin color. •They may be red due to the presence of vascular lesions or inflammation, or pigmented due to the Presence of melanin, hemosiderin, and drugs.
  • 4. Papule Solid lesions raised above the skin surface that are smaller than 1 cm in diameter. Papules may be seen in a wide variety of diseases including erythema multiforme simplex, rubella, lupus erythematosus, and sarcoidosis.
  • 5. Plaques Solid raised lesions that are over 1 cm in diameter; they are large papules.
  • 6. Nodules These lesions are present deep in the dermis,and the epidermis can be easily moved over them.
  • 7. Vesicles Elevated blisters containing clear fluid that are under 1 cm in diameter.
  • 8. Bullae Elevated blister like lesions containing clear fluid that are over 1 cm in diameter.
  • 9. Erosions Moist red lesions often caused by the rupture of vesicles or bullae as well as trauma.
  • 10. WHITE LESIONS
  • 11. A Non specific term used to describe any abnormal area of the oral mucosa that on clinical examination appears whiter than the surrounding tissue and is usually slightly raised ,roughened or of a different texture from adjacent normal tissue.
  • 12. Red Lesion Any area of reddened mucosa that may be smooth and atrophic looking or exhibits a granular, velvety texture
  • 13. Precancerous Lesions: defined as a morphologically altered tissue in which cancer is more likely to occur. e.g. Leukoplakia , Erythroplakia, Actinic chelitis, Palatal Changes with Reverse smoking. Precancerous condition: defined as a generalised state associated With significantly increased risk of cancer. e.g. Syphilis, OSMF, Siderophenic dysphagia, Erosive Lichen Planus, DLE.
  • 14. PREMALIGNANT CONDITION IN DETAILS  ORAL SUBMUCOUS FIBROSIS  ACTINIC KERATOSIS  DYSKERATOSIS CONGENITA  XERODERMA PIGMENTOSUM  PEUTZ JEGHERS SYNDROME  TERTIARY SYPHILIS  BOWEN’S DISEASE  EROSIVE LICHEN PLANUS  DISCOID LUPUS ERYTHEMATOUS PLUMMER VINSON SYNDROME
  • 15. White lesions classification            HEREDITARY WHITE LESIONS REACTIVE INFLAMATORY WHITE LESIONS INFECTIOUS WHITE LESIONS IDIOPATHIC TRUE LEUKOPLAKIA BOWENS DISEASE ORAL LICHEN PLANUS LICHENOID REACTIONS DEVELOPMENTAL- ECTOPIC LYMPHOID TISSUE FORDYCES GRANULES GINGIVAL CYSTS OF ADULT N NEW BORN MISCELLIANEOUS
  • 16. HEREDITARY WHITE LESIONS     LEUKODEMA WHITE SPONGY NEVUS HEREDITARY BENIGN INTRAEPITHELIAL DYSKERATOSIS DYSKERATOSIS CONGENITA
  • 17. REACTIVE INFLAMMATORY WHITE LESIONS         LINEA ALBA. FRICTIONAL KERATOSIS. CHEEK CHEWING. CHEMICAL INJURIES OF ORAL MUCOSA. ACTINIC KERATOSIS. SMOKELESS TOBACCO INDUCED KERATOSIS. NICOTINE STOMATITIS. SANGUINARIA INDUCED LEUKOPLAKIA
  • 18. DEVELOPMENTAL WHITE LESIONS —ECTOPIC LYMPHOID TISSUE FORDYCES GRANULES GINGIVAL CYSTS OF NEW BORN N ADULTS. MISSELLANEOUS LESIONS   GEOGRAPHIC TONGUE HAIRY TONGUE
  • 19. Lichen Planus
  • 20. Definition FITZ PATRICK et al-1993 defined Lichen Planus as a unique cutaneous entity consisting of an eruption of papules distinct in color and configuration, in patterns and location of appearance and in microscopic as well as gross structure.
  • 21. TYPES Reticular  Annular  Plaque(hypert rophic)  Papular  Erosive  Bullous  Atropic  Pigmented 
  • 22. ETIOLOGY Interplay of host,lifestyle and environmental factors Cell-mediated immunity initiated endogenous or exogenous factors. by
  • 23. EXOGENOUS/ENDOGENOUS FACTORS       Genetic Dental materials Drugs Infectious agents Auto immunity Immunodeficiency        Food allergy Stress Habits Trauma DM & HTN Malignancies IBD
  • 24. PATHOGENESIS Unknown Antigen enters OMM Antigen presentation by langerhans cells of OMM T.cell activation Increase in local cytokine production Intense inflammatory reaction Basal cell degeneration
  • 25. Basal cell degeneration Pyknotic and shrunken basal cells(civatte bodies) Apoptotic cell Phagocyotosed Incapable of phagocytosis Extruded into the underlying dermis(colloid bodies)
  • 26. CLINICAL FEATURES •Disease of middle aged,females and elderly •Except for erosive and Bullous forms all other forms are frequently painless and unrecognized by the patient. •About 50 % of patients have skin lesions •Skin lesions are flat-topped papules violaceous hue and a fine scaly surface. with
  • 27. RETICULAR FORM •Consists of slightly elevated,fine,whitish lines(wick ham's striae)that produce either a lace like lesion or a pattern of fine radiating lines(linear) or annular lesions. •Lesions are bi-lateral •Cheeks and tongue are commonly affected •Papular,plaque,atrophic and erosive lesions are frequently associated with reticular form.
  • 28. PAPULAR AND PLAQUE TYPE •0.5-1 mm whitish elevated areas or papules are usually seen,plaque like lesions are also seen that cannot be differentiated from leukoplakia. •Seen on keratinized and non-keratinized mucosa
  • 29. ATROPHIC •Appears as erythmatous areas surrounded by reticular elements. •Affects the gingiva also and gives a bright red edematous pattern involving the full width of attached gingiva(desquamative gingivitis)
  • 30. EROSIVE • Probably develop as a complication of atrophic process and not necessarily Bullous lesions. •Occurs more on the buccal mucosa •A pseudo membrane covers the lesion
  • 31. BULLOUS •Rarely observed form •Bullae and vesicles range from few mmseveral cm.,short-lived and rupture into ulcers. •Seen in postero-inferior aspect of the buccal mucosa •Striae to be seen here also.
  • 32. DIFFERENTIAL DIAGNOSIS Reticular-lichenoid reactions Plaque-leukoplakia,hyper plastic candidiasis,traumatic keratosis. Atrophic-speckled leukoplakia,anemic stomatitis,SLE and DLE. Erosive and Bullous-vesiculo-bullous lesions. Annular-erythema circinata migrans
  • 33. INVESTIGATIONS  HB%,CT & BT  Biopsy  Immunofluoroscence
  • 34. IMMUNOFLUOROSCENCE •Positive direct Immunofluoroscence, at the level of BM •Pattern may be globular or linear.
  • 35. TREATMENT Reasons to treat: Symptomatic cases Malignant potential(erosive LP)
  • 36. TREATMENT Asymptomatic Reassurance Symptomatic Treat
  • 37. SYMPTOMATIC CASES No Candida Candida Mild symptoms Mild symptoms Severe symptoms Topical steroid Systemic steroid + + Topical anti fungal Topical anti fungal Symptomatic maintenance with topical anti-fungal and topical steroids Topical steroid Ulcers resistant to heal Add intralesional steroids Severe symptoms Systemic steroid Symptomatic maintenance therapy
  • 38. TOPICAL STEROIDS •Triamcinalone acetate 0.01% •Clobetasol propionate •Flucinonide
  • 39. SYSTEMIC STEROIDS PREDNISOLONE 20-40 mg early morning once a day (taper gradually)
  • 40. OTHER MODALITIES Topical cyclosporine rinses Systemic azathioprine Levamisole(immuno modulator) Dapsone (immuno modulator) Surgery (lasers, cryo) Photo-chemo therapy(PUVA) Magneto therapy Reflexo therapy
  • 41. EROSIVE LICHEN PLANUS Malignant potential-2.7% Treat with topical/systemic vitamin A for reversal of dysplastic changes.
  • 42. OSMF
  • 43. DEFINITION An insidious chronic disease affecting any part of the oral cavity & sometimes the pharynx occasionally preceded by &/or assoc with vesicle formation and always assoc with juxtaepithelial inflammatory reaction,followed by a fibro elastic change of laminapropria with epithelial atrophy leading to stiffness of oral mucosa and causing trismus and inability to eat
  • 44. ETIOLOGY ARECANUT CHEWING WITH GENETIC PREDISPOSITION
  • 45. PATHOGENESIS Arecanut Arecoline(5-7%) Tannins(11-26%) Alkaloids(0.15-0.6%) Fibroblast proliferation Stimulates collagen synthesis Collagen fibrils resistant to human collagenase
  • 46. PATHOGENESIS ARECANUT ARECANUT CHEWING OSMF MUSCLE CONTRACTION JUXTA EPITHELIAL HYALINIZATION VASO OBLITERATION DIMINISHED BLOOD SUPPLY OVER ACTIVITY GLYCOGEN DEPLETION MUSCLE FATIGUE AND DEGENERATION FIBROSIS AND SCARRING OF THE MUSCLE
  • 47. CLINICAL FEATURES •Any age - 20 – 60 yrs predominantly •Male predominance
  • 48. Symptoms: •Burning sensation of the oral cavity aggravated by spicy/hot food/fluids •Vesiculation, excessive salivation, ulceration, pigmentation, recurrent stomatitis, defective gustatory sensations and dryness of mouth.
  • 49. •Gradual stiffening of oral mucosa after few yrs. •Difficulty in swallowing when fibrosis extends to pharynx and esophagus •Referred pain in ears, deafness and nasal voice
  • 50. SIGNS •Blanching appearance ,which to the imparts oral Marble-like mucosa.May be localized,diffused or lace -like network. •As disease progresses mucosa becomes stiff and vertical fibrous bands appear.
  • 51. In lip-circular bands appear. (Circum rima oris) In severe involvement of the lip-lips become leathery, difficult to avert In palate-bands radiate from the pterygomandibular raphe to the anterior faucial pillars. Faucial pillars - thin and short.
  • 52. •Tonsils- may be pressed between the faucial pillars. •Soft palate -Mobility is restricted when is involved. •Uvula-shrunken appearance bud like or hockey stick
  • 53. •Tongue-devoid of papillae, stiff with impaired protrusion in severe cases •Floor of the mouth-blanched and leathery •Petechiae seen in 1/5th of cases.
  • 54. CLINICAL AND FUNCTIONAL STAGING Haider et al 2000 BJOMS Clinical staging •Stage 1-faucial bands only •Stage 2-faucial and buccal bands •Stage 3-faucial,buccal and labial bands
  • 55. Functional staging •A –mouth opening >20mm •B-mouth opening 11-19 mm •C-mouth opening < 10 mm
  • 56. INVESTIGATIONS •Increased ESR •Anemia •Eosinophilia •Increased IgG •Decreased serum iron •Increased total Fe binding capacity •Decreased total saturation of transferrin •Decreased total serum iron
  • 57. Treatment Elimination of the habit Nutritional support Bland diet Cases without bands-topical corticosteroids Cases with bands-intra-lesional corticosteroids Physiotherapy Retinoids
  • 58. TREATMENT MODALITIES Intra lesional - cortico steroids Intra lesional - cortico steroids with hyalurinadase Systemic – Levamisole/Dapsone Soft lasers Turmeric oil Homeopathy(calcaria florica)
  • 59. Formulations and dosage Dexamethasone – 2ml (1ml on each side surrounding the bands)-biweekly for 10 weeks Hydrocortisone – 1.25 ml once a week for 12 weeks Dexamethasone – 2ml+hyalurinadase 1500 IU,biweekly for 10 weeks  Hydrocortisone – 1ml+ hyalurinadase 1500 IU,biweekly for 10 weeks
  • 60. ACITINIC(SOLAR) KERATOSIS/ELASTOSIS / CHELITIS
  • 61. DEFINITION IS A PREMALIGNANT SQUAMOUS CELL LESION DUE TO LONG TERM EXPOSURE TO SOLAR RADIATION.
  • 62. CLINICAL FEATURES •Seen on skin,Vermillion border of the lip as a crusted and Keratotic lesion. •Labial mucosa exposed to the sun- white area of atrophic epithelium develops underlying scarring of lamina propria( referred to as Elastosis ) •Malignant transformation (10%)
  • 63. TREATMENT Topical 5-fluoro uracil Surgical lip shaving procedures Topical steroids in between treatments to control lip swelling
  • 64. LEUKOEDEMA
  • 65. Occurs in 15-35 yrs old. M:F =2:1 Highest in Blacks(USA),lowest in Indians The buccal mucosa exhibiting a grayish- white ,slightly folded ,opalescent appearance with normal softness and flexibility is termed leukodema. This change temporarily eliminated by stretching the mucosa,but re-establishes itself immediately. Melanin pigmentation enhances opalescence
  • 66. LINEA ALBA BUCCALIS
  • 67. The line of keratinization usually found on the non-keratinized buccal mucosa parallel to the line of occlusion and expanding to a triangular area in the retro-commisure.
  • 68. FORDYCE’S GRANULES
  • 69. FORDYCE’S GRANULES
  • 70. Ectopic presence of tubulo-acinar sebaceous glands in oral cavity. Appears in 80-90 % of adult population. Appears plaques. as small ,white/yellowish sub-mucosal
  • 71. Seen on Vermillion border, buccal mucosa, occasionally on the palate , gingiva and the tongue. No specific function/does not increase with age. Occasionally transforms cyst/sebaceous adenoma. into pseudo
  • 72. WHITE SPONGY NEVUS  Etiopathogenesis : Mutations in Genes Coding For Epihtelial Keratin Of Type K4 N K33.  :Clinical features:  Age:18 –22yrs….  M=f.Autosomal Dominant Disorder….  Site : Buccal Mucosa.  Extra Oral Sites : Oesophagus,anogenital Mucosa.  .Management: No Specific Treatment Required.
  • 73. WHITE SPONGY NEVUS
  • 74. NICOTINE STOMATITIS  ETIOLOGY: HEAVY CIGARETTE ,PIPE ,CIGAR SMOKING.  C/F:NUMEROUS ELEVATED PAPULES WITH RED PUNCTATED CENTER…… INFLAMMED SALIVARY GLAND WITH ALTERED DUCTS.  HISTOPATH:HYPERKERATOSIS,SQUAMOUS METAPLASIA,MILD TO MODERATE INFLAMMTION. .
  • 75. NICOTINE STOMATITIS
  • 76. MEDIAN RHOMBOID GLOSSITIS
  • 77. LEUKOPLAKIA
  • 78. NAME GIVEN BYSCHIERMER GREEK WORD- Leucos means patch. means white and plakia
  • 79. Definition It is a predominantly white lesion of the oral mucosa that cannot be characterized as any other definable lesion ,some oral Leukoplakia’s will transform into cancer
  • 80. CLASSIFICATION AXELL.T. et al (1996) Homogenous Non homogenous Erythroplakia
  • 81. ETIOLOGY Tobacco
  • 82. PATHOGENESIS Tobacco(chemical constituents and combustion products such as tars and resins) + additional effect of heat from the burning of tobacco Irritation of oral mucosa producing leukoplakic changes.
  • 83. PREDISPOSING FACTORS Alcohol Vitamin deficiency Candida Viruses
  • 84. CLINICAL FEATURES Three types : Homogenous Nodular/Granular/Speckled/Non-homogenous Verrucous
  • 85. CLINICAL FEATURES Age – average 60 yrs(less than 20 also recorded) Sex – M:F = 3:2 Site – although leukoplakia can be found in any location,buccal mucosa,gingivae and Vermillion border of the lip are involved.Lips,palate,retro molar area ,floor of the mouth,tongue are less likely sites.
  • 86. CLINICAL FEATURES •Homogenous refers to a localized lesion or an extensive white patch that presents a relatively consistent pattern throughout ,even though the surface of the lesion may be described variously as corrugated(ebbing tide),with a pattern of fine lines(cristae),wrinkled(dry-cracked mud)or papillomatous.
  • 87. CLINICAL FEATURES Nodular leukoplakia refers to a mixed red and white lesion with small Keratotic nodules are scattered over an atrophic patch of mucosa
  • 88. CLINICAL FEATURES Verrucous leukoplakia is one in which the surface is broken up by multiple papillary projections that may also be heavily keratinized producing a lesion that bears some resemblance to the dorsum of the tongue.
  • 89. INVESTIGATIONS SMEAR-to rule out candidal involvement Toludine blue application. Biopsy
  • 90. DIFFERENTIAL DIAGNOSIS HOMOGENOUS CANDIDAL LEUKOPLAKIA SYPHILITIC WHITE PATCH CRYPTOGENIC LEUKOPLAKIA LEUKOPLAKIA INDUCED BY GALVANISM,TRAUMA,ETC. PLAQUE TYPE LICHEN PLANUS SPECKLED ATROPHIC LICHEN PLANUS
  • 91. MALIGNANT POTENTIAL Over all : 3-6% Type wise : Homogenous 0.5-1.7 % Speckled 20% Site wise : Floor of the mouth - highest
  • 92. TREATMENT Stop the habit Topical anti fungal for 2 weeks Biopsy and topical Vit A application Beta carotene 5000 IU/day(chemo prevention)
  • 93. GUIDELINES FOR MANAGEMENT Clinical observation without biopsy is dangerous Response to hyperkeratotic leukoplakia is unpredictable,so biopsy to be repeated every 6 – 12 months particularly if the lesion changes in size or physical characteristics. Adequate follow up,especially for nodular,Verrucous forms and leukoplakia at the floor of the mouth and tongue.
  • 94. TREATMENT(other modes) Topical Bleomycin Cryo surgery Laser ablation Surgical stripping with graft coverage
  • 95. CANDIDIASIS
  • 96. DEFINITION Infection caused by fungus CANDIDA
  • 97. CLASSIFICATION Candidiasis Secondary Primary Acute chronic Candidaassociated lesions
  • 98. ORAL CANDIDIASIS Acute : Pseudomembranous Erythematous(atrophic) Chronic : Pseudomembranous Erythematous Plaque like Nodular Candida associated : lesions Denture stomatitis Angular chelitis Median rhomboid glossitis
  • 99. secondary         Familial chronic mucocutaneous candidiasis Diffuse chronic mucocutaneous candidiasis Candidiasis endocrinopathy syndrome Familial mucocutaneous candidiasis Severe combined immunodeficiency DiGeorge syndrome Chronic granulomatous disease Acquired immune deficiency syndrome (AIDS)
  • 100. PREDISPOSING FACTORS Marked changes in the oral microbial flora Broad spectrum antibiotics Excessive use of anti microbial mouth rinses. Xerostomia secondary to anticholinergic agents and SG disease.
  • 101. Chronic local irritants. Dentures Orthodontic appliances Heavy smoking
  • 102. PREDISPOSING FACTORS Administration of cortico steroids (topical,oral,inhalation & systemic) Radiation to head and neck Age (infancy,pregnancy,old age) Hospitalization age, debilitating diseases,antibiotics)
  • 103. CLINICAL FEATURES PSEUDOMEMBRANOUS CANDIDIASIS Superficial infection of the upper layer of the epithelium,resulting in the formation of patchy white flecks. Surrounding mucosa-may /may not be reddened.Plaque removal ,by rubbing or scraping shows erythema/shallow ulceration.
  • 104. Transient episodes of thrush may occur as isolated prominences that disappear spontaneously with minimum/no treatment. Common neonates and children.
  • 105. Typical lesion of infants-soft white or bluish white,adherent patches on the oral mucosa at times,extending to circum oral tissues. Lesions are painless Can be removed with tissue difficultly,leaving raw bleeding surfaces.
  • 106. In adultsLesions may evolve beneath dentures or any other area of the oral cavity. Inflammation,erythema and painful eroded may more be more often associated with. Entire oral mucosa may be involved. Mild symptoms compared to other stomatitis’ Burning of mouth and throat precede in antibiotic therapy predisposed.
  • 107. CHRONIC PLAQUE TYPE
  • 108. CHRONIC NODULAR TYPE
  • 109. DIFFERENTIAL DIAGNOSIS Flecks of milk Flecks of food debris Antacids remaining on the oral mucosa ,esp. in infants. Debilitated elderly patient ( intern’s thrush ) Cheek biting Chemical burn
  • 110. ERYTHEMATOUS(ATROPHIC) Includes antibiotic sore mouth. Red pattern of raw atrophic mucosa persists with no evidence of pseudomembranes. Generalized depapillation of tongue. Palate and buccal mucosa can be involved. Pt develops symptoms of bad taste,oral burning,sore throat during convalescent periods of illness,treated with broad – spectrum antibiotics.
  • 111. ERYTHEMATOUS(ATROPHIC)
  • 112. HYPERPLASTIC CANDIDIASIS Chronic disease Raised lesions that vary from small,palpable,translucent areas whitish areas to large dense opaque plaques which are hard and rough to touch. Homogenous/Speckled/Nodular areas which do not rub off.  3- 50 % of candida –hyperplastic.
  • 113. Treatment  Nystatin  Cream Apply to affected area.  Oral suspension, Apply after meals 4x/d, usually for 7 d, 100,000 U continue use for several days after post clinical healing Candid -B cream 
  • 114. ASSOCIATED LESIONS CHRONIC ATROPHIC / DENTURE SORE MOUTH
  • 115. AETIOLOGY •Traumatic : Irritation is the foremost etiology. Inadequate,ill fitting dentures, abnormal movements •Toxic: Chemical action of free monomer Poor denture hygiene Putrefaction of chemical food
  • 116. •Allergic : Hypersensitivity to denture material •Infections : Nonspecific bacteria, candidal species •Malnutrition: Alcoholism, DM (uncontrolled) Anemia's •Idiopathic: Resistance to treatment •Stomatitis with palatal inflammatory hyperplasia
  • 117. CLINICAL FEATURES Palatal hyperplasia Palatal mucosa – velvety or may resemble an over ripe berry and bleed on slight pressure. Pain and burning Intensely reddened ,glistening and slightly
  • 118. Denture Stomatitis
  • 119. ANGULAR CHELITIS/STOMATITIS
  • 120. DEFINITION Any inflammatory lesion of the corner of the mouth.
  • 121. AETIOLOGY MALNUTRITION MECHANO-TOXICITY INFECTION TRAUMA ALLERGY IDIOPATHIC
  • 122. CLINICAL FEATURES Intensely red,fissured,eroded or ulcerated areas Generally accompanied by symptoms of soreness,tenderness,burning or frank pain.
  • 123. Malnutrition induced •Intensely red in the muco-cutaneous junction surrounding the skin. •Fissures and superficial erosion on an inflamed base •Ulceration coated with Greyish-white or yellow membrane or exudate.
  • 124. Mechano-toxic variety Loss of intermaxillary distance Closure of bite,acceleration of transverse folds of skin at the angle of the mouth. Saliva drools out at the corners Fluids deposited leaves accentuated folds. Drying of saliva and formation of irritating end- products Inflammation
  • 125. Infection type : Strepto/Staphylo/Candida Traumatic type : Dental procedures Allergy/toxic : Cosmetics/lipsticks/ointments Idiopathic : Metabolism/Harmonal/Emotional
  • 126. INVESTIGATIONS MICROBIOLOGY: •Smear from the lesion Grams/PAS •Swab : cotton dipped swab •Imprint culture •Saliva culture HISTOPATHOLOGY Biopsy IMMUNOLOGICAL TESTS •Candida agglutination,precipitation immunoflorescence •ELISA HEMATOLOGY TLC,DC,Folate,Vit B 12,Serum Ferritin
  • 127. TREATMENT Topical antifungal : Clotrimazole( Azoles ) Ketaconazole :200 mg x 7 days Fluconozole : 50 mg O.D x 10 days Intraconozole : 100 – 200 mg/day x 2 weeks DNA Analogues : Flucytomine 50 – 150 mg/kg/day x quad/day(divided doses ) Amphoterecin 100 mg/ml

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